During AP, the massive release of inflammatory factors such as tumor necrosis factor α (TNF-α) cause intestinal mucosa damage, and these factors can further promote the activation of inflammatory mitogen-activated protein kinase (MAPK) and nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing 3 (NLRP3) pathways and the release of inflammatory mediators, leading to more severe intestinal inflammation [5–7]. The gene discussed is TNF; the disease is alkaline phosphatase measurement.